Submitted to: Society for Leukocyte Biology Meetings Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 7/14/1998
Publication Date: N/A
Citation: N/A Interpretive Summary:
Technical Abstract: In previous work, feeding mice beta-glucan at 0.050% of their diet increased survival during a STREPTOCOCCUS SUIS challenge. Increased serum IL-1 and a trend for increased IL-1 type II receptors on macrophages were associated with 0.025% dietary concentration of beta-glucan while those fed 0.050% had IL-1 and IL-1 receptor type II concentrations similar to controls. Objectives of this research were to determine how dietary concentrations of beta-glucan influence IL-1 receptor antagonist (IL-1Ra) production in mice and to determine in which tissues beta-glucan contacts immune cells. Serum IL-1Ra increased significantly in all mice fed beta-glucan for 28 d. Therefore, feeding 0.050% beta-glucan, the treatment which improved survival, decreased the ratio of IL-1:1L-1 RA. To determine where beta-glucan particles may be interacting with immune cells, we injected 3 mice i.p. with FITC labeled beta-glucan and control mice with saline. After 24 hr. tissues were aliquoted into 3 tubes. The first tube was analyzed for FITC, the next two tubes were labeled with PE labeled anti-CD69 (very early activation marker) and PE labeled anti-CD80 (expressed on antigen presenting cells). The greatest increase of FITC fluorescence occurred in thymus (35.4% more than controls) and lung (25.1% more than controls) cells. Spleen cells increased only 9.4% and liver and bone marrow cells did not differ from control cells. Lung cell expression of CD69 and CD80 increased (66.3% and 80.1%, respectively) with beta-glucan. Thymocytes modestly increased CD69 and CD80 expression (22.1 and 13.0%, respectively). These results demonstrated movement of beta-glucan predominantly to the thymus and lungs and suggest a protective effect of deceased IL-1 to IL-1Ra ratio by 0.050% oral beta-glucan.